Evidence map›Paper›PMID 34666219›Full record

ArticleBiomedical journal2022

Brain stem death induces pro-inflammatory cytokine production and cardiac dysfunction in sheep model.

K Walweel, A C Boon, L E See Hoe, N G Obonyo, S E Pedersen, S D Diab, M R Passmore, K Hyslop, S M Colombo, N J Bartnikowski and 15 more

Open access · goldAbstract read
In one paragraph

Article in Biomedical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 37% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. A concerted effort combating hepatitis.Biomedical journal · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

25 authors at 6 institutions in 3 countries.

K WalweelCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia. Electronic address: k.walweel@uq.edu.au.
A C BoonCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
L E See HoeCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
N G ObonyoCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia; Initiative to Develop African Research Leaders, KEMRI-Wellcome Trust Research Programme, Kilifi, Kenya.
S E PedersenCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
S D DiabCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
M R PassmoreCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
K HyslopCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
S M ColomboCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia; University of Milan, Italy.
N J BartnikowskiQueensland University of Technology, Australia.
M BouquetCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
M A WellsCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia; School of Medical Science, Griffith University, Australia.
D M BlackCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
L P PimentaCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
A K StevensonCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
K BishtMater Research Institute, University of Queensland, Australia.
K SkeggsCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia; Princess Alexandra Hospital, Woolloongabba, Brisbane, Australia.
L MarshallPrincess Alexandra Hospital, Woolloongabba, Brisbane, Australia.
A PrabhuThe Prince Charles Hospital, Rode Road, Brisbane, Australia.
L N JamesPrincess Alexandra Hospital, Woolloongabba, Brisbane, Australia.
D G PlattsCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia.
P S MacdonaldCardiac Mechanics Research Laboratory, St. Vincent's Hospital and the Victor Chang Cardiac Research Institute, Victoria Street, Darlinghurst, Sydney, Australia.
D C McGiffinCardiothoracic Surgery and Transplantation, The Alfred Hospital, Melbourne, Australia.
J Y SuenCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia. Electronic address: j.suen1@uq.edu.au.
J F FraserCritical Care Research Group, Level 3, Clinical Sciences Building, The Prince Charles Hospital, Rode Road, Brisbane, Australia. Electronic address: fraserjohn001@gmail.com.
Prince Charles Hospital · AUPrincess Alexandra Hospital · AUQueensland University of Technology · AUSt Vincent's Hospital Melbourne · AUThe Alfred Hospital · AUThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionOrgans procured following brain stem death (BSD) are the main source of organ grafts for transplantation. However, BSD is associated with inflammatory responses that may damage the organ and affect both the quantity and quality of organs available for transplant. Therefore, we aimed to investigate plasma and bronchoalveolar lavage (BAL) pro-inflammatory cytokine profiles and cardiovascular physiology in a clinically relevant 6-h ovine model of BSD.

methodsTwelve healthy female sheep (37-42 Kg) were anaesthetized and mechanically ventilated prior to undergoing BSD induction and then monitored for 6 h. Plasma and BAL endothelin-1 and cytokines (IL-1β, 6, 8 and tumour necrosis factor alpha (TNF-α)) were assessed by ELISA. Differential white blood cell counts were performed. Cardiac function during BSD was also examined using echocardiography, and cardiac biomarkers (A-type natriuretic peptide and troponin I were measured in plasma.

resultsPlasma concentrations big ET-1, IL-6, IL-8, TNF-α and BAL IL-8 were significantly (p < 0.01) increased over baseline at 6 h post-BSD. Increased numbers of neutrophils were observed in the whole blood (3.1 × 10

conclusionsBSD induced systemic pro-inflammatory responses, characterized by increased neutrophil infiltration and cytokine production in the circulation and BAL fluid, and associated with reduced heart contractile function in ovine model of BSD.

Indexed as

Heart DiseasesTumor Necrosis Factor-alphaAnimalsBrain StemCytokinesFemaleInterleukin-8SheepCytokinesInterleukin-8Tumor Necrosis Factor-alphaBrain stem deathCytokinesEndothelin-1InflammationTransplantationTroponin

Identifiers

PMID34666219
PMCPMC9661508
OpenAlexW3206033743

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.